The objective of this study was to assess long-term clinical outcomes and their correlates in medically managed outpatients with stable angina pectoris, healed myocardial infarction (MI), or documented asymptomatic coronary artery disease (CAD). Management strategy emphasized maximally tolerated medical therapy and modification of coronary risk factors. Referral to invasive coronary interventions followed stricter criteria than standard published guidelines. Primary study outcomes were all-cause mortality or nonfatal myocardial infarction. Secondary study outcomes included cardiac death, unstable angina, or coronary revascularization. A total of 693 men and women with proved CAD (mean age 67 years at entry, 85% men, 41% with history of MI) were enrolled. The annual incidence of nonfatal MI, cardiac mortality, and total mortality was 2.2%, 0.8%, and 1.4%, respectively, during an average follow-up of 4.6 years. Coronary revascularization was performed in 24% of subjects; unstable or progressive anginal symptoms were the most common reasons for revascularization. In patients with documented stable CAD, a management strategy based on intensive medical therapy and modification of established coronary risk factors was associated with excellent long-term outcomes. Thus, coronary interventions can be safely delayed until clinical instability ensues, without increased risk of MI or death. This treatment approach represents a viable alternative to invasive strategies.
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http://dx.doi.org/10.1016/j.amjcard.2003.10.007 | DOI Listing |
Alzheimers Dement
December 2024
Karolinska Institute, Stockholm, Södermanland and Uppland, Sweden.
Background: Novel anti-amyloid therapies (AAT) for Alzheimer's Disease (AD) have recently been approved in the United States, Japan and China, and are under regulatory review in Europe. Questions remain regarding the long-term effectiveness and value of these drugs when used in routine clinical practice. Data from follow-up studies will be important to inform their optimal use, including criteria for treatment initiation, monitoring strategies, stopping rules, pricing and reimbursement considerations.
View Article and Find Full Text PDFBackground: Seizures in Alzheimer's Disease (AD) are increasingly recognized to occur and can increase cognitive decline and reduce survival compared to unaffected age-matched peers (Lyou et al. 2018). Administration of antiseizure medicines (ASMs) to AD patients with epileptiform activity may improve cognition (Vossel et al.
View Article and Find Full Text PDFClin Appl Thromb Hemost
January 2025
Department of Pharmacy Practice, College of Pharmacy, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.
Deep vein thrombosis (DVT) is a leading cause of death disability. DVT can be classified based on the location and extent of the clot into isolated distal DVT (iDDVT), isolated proximal DVT (iPDVT), or mixed DVT. The aim of this study is to explore the baseline characteristics and clinical outcomes of patients with different types of DVT.
View Article and Find Full Text PDFBackground: Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein. In clinical studies, lecanemab has been shown to reduce markers of amyloid in early symptomatic Alzheimer's disease (AD) and slow decline on clinical endpoints of cognition and function. Herein, a modeling approach was used to correlate amyloid reduction with change in rate of AD progression.
View Article and Find Full Text PDFA 10 mg/kg every 2 week (Q2W) dose of the humanized IgG1 monoclonal antibody lecanemab was approved after demonstrating significant clinical benefit in slowing cognitive decline in early Alzheimer's disease (AD) in two clinical studies (the phase 2 Study 201 and phase 3 Clarity AD). A less frequent every 4 weeks lecanemab 10 mg/kg maintenance dosing (Q4W) has been proposed after a sufficient initial Q2W treatment. To further understand long-term benefit of continued Q4W lecanemab treatment, a quantitative systems pharmacology (QSP) model was developed which mechanistically describes AD pathophysiology using multivariate data from clinical studies.
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